Identification of a DNA methylation-independent imprinting control region at the Arabidopsis MEDEA locus

Abstract

Genomic imprinting is exclusive to mammals and seed plants and refers to parent-of-origin-dependent, differential transcription. As previously shown in mammals, studies in Arabidopsis have implicated DNA methylation as an important hallmark of imprinting. The current model suggests that maternally expressed imprinted genes, such as MEDEA (MEA), are activated by the DNA glycosylase DEMETER (DME), which removes DNA methylation established by the DNA methyltransferase MET1. We report the systematic functional dissection of the MEA cis-regulatory region, resulting in the identification of a 200-bp fragment that is necessary and sufficient to mediate MEA activation and imprinted expression, thus containing the imprinting control region (ICR). Notably, imprinted MEA expression mediated by this ICR is independent of DME and MET1, consistent with the lack of any significant DNA methylation in this region. This is the first example of an ICR without differential DNA methylation, suggesting that factors other than DME and MET1 are required for imprinting at the MEA locus.

Kin Conflict in Seed Development: An Interdependent but Fractious Collective

“…Consistent with these predictions, seeds with maternal dme mutations have enlarged endosperm (Choi et al 2002) whereas seeds with paternal met1 mutations produce small, precociously cellularized, endosperm (Xiao et al 2006). A simple story in which DME and MET1 combine to establish different epigenetic states of maternal and paternal chromosomes cannot explain all imprinting in Arabidopsis endosperm because imprinted expression of MEA and a large class of small-interfering RNAs is maintained in the presence of maternal dme and paternal met1 mutations (Mosher et al 2011;Wöhrmann et al 2012). …”

“…A 200-bp sequence is necessary and sufficient for imprinted expression of MEA (Wöhrmann et al 2012). MEA protein binds directly to MEA promoters and reduces transcription of maternal MEA alleles in endosperm.…”

The Armadillo Repeat Gene ZAK IXIK Promotes Arabidopsis Early Embryo and Endosperm Development through a Distinctive Gametophytic Maternal Effect

“…Activation of the maternal MEA allele involves the DNA glycosylase DEMETER (DME), disruption of which leads to a GME seed abortion phenotype (Choi et al, 2002;Jullien et al, 2006b). Paternal silencing of MEA, FIS2, and FIE is directly or indirectly regulated by DNA methylation mediated by DNA METHYLTRANSFERASE1 (MET1) or DECREASED DNA METHYLATION1 (DDM1) (Vielle-Calzada et al, 1999;Vinkenoog et al, 2000;Yadegari et al, 2000;Jullien et al, 2006b;Wöhrmann et al, 2012) and trimethylation of histone H3 Lys-27 (H3K27me3), which is deposited by FIS-PRC2 (Baroux et al, 2006;Gehring et al, 2006;Jullien et al, 2006b).…”

Emerging links between iron-sulfur clusters and 5-methylcytosine base excision repair in plants

“…Data from isolated CCs indicating that the FWA promoter may be highly methylated in differentiated CCs ( Fig. 2i; Wohrmann et al, 2012) cannot currently be reconciled with the rest of the findings.…”